共查询到20条相似文献,搜索用时 328 毫秒
1.
Formation of {3H}-PGF2α and {3H}-13,14,dihydro-15-keto-PGF2α from {3H}-PGE2 by the supernatant of uterine homogenates from estrous and ovariectomized rats, was studied, using the reaction system PGE2 + NADPH + {3H}-PGE2 + supernatant. Enzymatic conversion was lower in uterine supernatants from spayed rats than in uterine homogenates of rats at natural estrus.Spayed animals were injected with progesterone (P) or with estradiol-17-β (E0) at a dose of 1.0 or 50.0 ug. Conversion of {3H}-PGF2α to {3H}-PGE2 or to {3H}-13,14,dihydro-15-keto-PGF2α did not differ in control ovariectomized or ovariectomized rats receiving P or 1.0 ug E0. However, 50.0 ug E0 induced a significant oversion after 30 (P < 0.01) and 60 (P < 0.001) min of incubation.It is concluded that E0, at the 50.0 ug dose, but not the 1.0 ug dose of E0, nor progesterone, stimulated conversion of {3H}-PGE2 into {3H}-PGF2α or {3H}-13, 14,dihydro-15-keto-PGF2α, presumably through the activity of the enzyme PGE2-9-keto-reductase. 相似文献
2.
The catabolism
of prostaglandin F2α(PGF2α) in rat ovarian homogenate was studied comparing with uterine homogenate. Two kinds of metabolite were recognized by incubation of PGF2α with ovarian or uterine homogenate; 13,14-dihydro-15-keto-PGF2α(15KD-PGF2α) and 13,14-dihydro-PGF2α(13,14H2-PGF2α) in ovarian homogenate and 15-keto-PGF2α(15K-PGF2α) and 15KD-PGF2α in uterine homogenate. Incubation of 15KD-PGF2α with ovarian homogenate resulted in the formation of 13,14H2-PGF2α but incubation with uterine homogenate did not produce 13,14H2-PGF2α. 13,14H2-PGF2α was in accord with Rf value of a compound formed by reduction of 15KD-PGF2α with sodium borohydride. 相似文献
3.
T. Obata T. Nagakura M. Kammuri T. Masaki K. Maekawa K. Yamashita 《Journal of chromatography. B, Analytical technologies in the biomedical and life sciences》1994,655(2)
Sensitive and specific assay methods for 9α,11β-prostaglandin F2 (9α,11β-PGF2) by gas chromatography—mass spectrometry with electron impact ionization are described. The mass spectrometric assay for 9α,11β-PGF2 was based on the use of the methyl ester—dimethylisopropylsilyl ether derivative, and pentadeuterated PGF2α as a convenient internal standard. The calibration graph for 9α,11β-PGF2 was linear from 5 pg to 100 ng for both the standard and spiked biological samples. The limit of detection was 50 pg/ml for urine and 25 pg/ml for plasma (signal-to-noise RATIO = 2.3). The method was applied to the determination of 9α,11β-PGF2 in urine and plasma samples from patients with bronchial asthma. 相似文献
4.
C.H. Spilman D.C. Beuving A.D. Forbes F.A. Kimball 《Prostaglandins & other lipid mediators》1977,14(3):477-488
The effects of prostaglandin (PG)F2α and PGF2α, 1–15 lactone were compared in luteal phase, non-pregnant and in early pregnant rhesus monkeys. Animals treated with either PG after pretreatment with human chorionic gonadotropin (hCG) had peripheral plasma progesterone concentrations that were not statistically different from those in animals treated with hCG and vehicle. However, menstrual cycle lengths in monkeys treated with PGF2α, 1–15 lactone were significantly (P <0.02) shorter than those in vehicle treated animals. In the absence of hCG pretreatment, plasma progesterone concentrations were significantly (P <0.008) lower by the second day after the initial treatment with either PGF2α or PGF2α, 1–15 lactone than in vehicle treated monkeys. Menstrual cycle lengths in monkeys treated with either PG were significantly (P <0.04) shorter than those in animals treated with vehicle. There were no changes in plasma progesterone concentrations in early pregnant monkeys treated with PGF2α, and pregnancy was not interrupted. In contrast, plasma progesterone declined and pregnancy was terminated in 5 of 6 early pregnant monkeys treated with PGF2α, 1–15 lactone. These data indicate that PGF2α, 1–15 lactone decreases menstrual cycle lengths in non-pregnant rhesus monkeys. More importantly, PGF2α, 1–15 lactone terminates early pregnancy in the monkey at a dose which is less than an ineffective dose of PGF2α. 相似文献
5.
The mechanism of stimulatory and inhibitory action of PGF2α on ovarian steroidogenesis both under
and
conditions has been studied in the pseudo-pregnant rabbits. Short term incubation of the ovaries with PGF2α (2.82 × 10−5M) resulted in an increased synthesis of progesterone and 20α-OH P. The addition of PGF2α in the medium and further incubation of the ovaries obtained from rabbits that had been constantly infused with PGF2α (0.5 μg/min.) for two hours resulted in increased synthesis of these progestins. The ratio of progesterone to 20α -OH P was also enhanced under these conditions and thus supported the luteotropic action of small doses of PGF2α under short term incubations. However, as the amount of PGF2α infused was increased to 5 μg/min., the addition of PGF2α under
conditions strikingly decreased the production of these progestins. The ratio of progesterone to 20α -OH P was also decreased and thus was indicative of luteolytic action of higher doses of PGF2α. High doses of PGF2α (5.64 × 10−4M) failed to I cause any significant change in the progestin synthesis under short term incubation. These results thus suggest that the luteotropic and luteolytic action of PGF2α in the luteinized rabbit ovary is dose and time dependent. 相似文献
6.
Ray V. Haning Jr. Leslie Choi Amber J. Kiggens Donna L. Kuzma John W. Summerville 《Prostaglandins & other lipid mediators》1982,23(1):29-40
Explants from term human placentas were maintained in culture with daily changes of medium. Daily output of PGF2α and PGFM1 decreased during the course of the incubation. Addition of 4 μg/ml DHEAS or 67 μg/ml LDL cholesterol had no effect on output of PGF2α or PGFM. Addition of 1.6, 3.2, or 6.4 μg/ml of LHRH to the culture plates had no effect on output of PGFM or PGF2α, but LHRH increased hCG output. Dibutyryl cAMP (1mM, 2mM, and 4mM) increased output of PGF2α, PGFM, and hCG. Aromatase inhibitor decreased hCG output, but it was without effect on output of PGF2α, or PGFM. Significant correlations were demonstrated between progesterone, PGFM, PGF2α, and hCG, suggesting that PGF2α originates in the syncytiotrophoblast cell. The ability of LHRH to stimulate output of hCG but not PGF2α while dbcAMP stimulated both suggests that either PGF2α and hCG arise in different cells or that LHRH does not act through cAMP. 相似文献
7.
Ovine luteal slices were used to study the effects of prostaglandins (PG) F2α on luteinizing hormone (LH)-stimulated secretion of progesterone and adenylate cyclase activity. The accumulation of progesterone in incubation medium and adenylate cyclase activity was similar after incubation of luteal slices with Medium 199 alone or Medium 199 containing PGF2α (250 ng/ml) for 3 hr. Addition of luteinizing hormone (LH; 100 ng/ml) resulted in a 2–3 fold increase in both the rate of progesterone accumulation and adenylate eyclase activity by 3 hr. When luteal slices were incubated in the presence of both LH and PGF2α the rates of progesterone accumulation and adenylate cyclase activity were identical to those in flasks containing LH alone after 1 hr; however, after 3 hr both LH stimulated progesterone accumulation and adenylate cyclase activity were inhibited to levels similar to those observed in control slices.In a second experiment, after 60–120 min of exposure to PGF2α the rate of progesterone accumulation in the medium was not different from that in untreated control slices. In addition, after this experiment the luteal slices were homogenized and the basal, sodium fluoride, LH, isoproterenol (ISO) and PGE2 sensitive adenylate cyclase activities were determined to evaluate the hormonal specificity of the negative effect of the pretreatment with PGF2α. Both LH and ISO stimulated adenylate cyclase activities were reduced after PGF2α pretreatment. However, fluoride ion stimulated adenylate cyclase activity was not significantly effected by PGF2α pretreatment and PGE2 sensitive adenylate cyclase was effected only slightly. 相似文献
8.
M. Viggiano A.M. Franchi A. Faletti M.A.F. Gimeno A.L. Gimeno 《Prostaglandins & other lipid mediators》1988,36(3)
The effects of exogenous histamine (H) on prostaglandin (PG) generation and release in uteri isolated from diestrous rats and the influences of H2-receptors blockers (cimetidine and mitiamide) on the output of uterine PGs, were explored. Moreover, the action of H on the uterine 9-keto-reductase, was also studied. Histamine (10−4M) failed to alter the basal output of PGE1 but reduced significantly the generation and release of PGE2 and augmented the output of PGF2α. On the other hand, cimetidine (10−5M) enhanced the basal release of PGE2 but had no action on the outputs of PGs E1 or F2α. The enhancing effect of H on the production and release of PGF2α was abolished in the presence of cimetidine. Also, the antagonist reversed the influence of H on the output of PGE2. Metiamide, another H2-receptor antagonist, did not alter the basal control generation and release of uterine PGs, but antagonized the augmenting influence of H on PGF2α uterine output, as much as cimetidine did, and prevented the depressive action of H on the release of PGE2 from uteri. Histamine (10−4M) significantly stimulated uterine formation of cyclic-adenosine monophosphate, an action which was antagonized by the presence of cimetidine (10−5M), a blocker of H2 receptors. Also, histamine (10−5M) and dibutyril-cyclic-adenosine monophosphate (DB-cAMP) at 10−3M, enhanced significantly the formation 3H-PGF2α from 3H-PGE2. Results presented herein demonstrate that H is able to diminish the generation of PGE2 in uteri from rats at diestrus augmenting the synthesis of PGF2α, apparently via the activation of H2-receptors, enhancing adenylate-cyclase. These effects appear to increase uterine 9-keto-reductase activity which transforms PGE2 into PGF2α. Relationships between the foregoing results and those evoked by estradiol, are also discussed. 相似文献
9.
Lawrence Levine Kung-Yue Wu Sheng-Shung Pong 《Prostaglandins & other lipid mediators》1975,9(4):531-544
Antibodies directed toward PGF2β were prepared in rabbits. The serologic specificity of the immune reaction was determined by inhibition of sodium borohydride-reduced (3H) PGE2 anti-PGF2β binding by several prostaglandins. The antibodies to PGF2β recognize the β-hydroxyl configuration in the cyclopentane ring of PGF2β. With the use of both anti-PGF2α and anti-PGF2β, the product of PGE2 reduction by 9-ketoreductase purified from chicken heart was identified as PGF2α. Guinea pig liver and kidney homogenates were examined for PGE 9-ketoreductase activity. Although enzyme activity was present, no evidence of PGF2β production was found. 相似文献
10.
G.J. Wiepz M.C. Wiltbank S.B. Kater G.D. Niswender H.R. Sawyer 《Prostaglandins & other lipid mediators》1993,45(2)
When ovine large luteal cells are placed in culture and exposed to PGF2α, there is a rapid and sustained increase in the concentration of free intracellular calcium which is believed to play a major role in the luteolytic and cytotoxic effects of PGF2α. Since administration of exogenous PGE2 can prevent spontaneous and PGF2α-induced luteolysis in vivo, and the cytotoxic effects of PGF2α on large luteal cells in vitro, the objective of this study was to determine if one mechanism by which PGE2 acts is to attenuate increases in free intracellular calcium induced by PGF2α. At concentrations of 10 nM or greater, PGF2α caused a significant and sustained increase in free intracellular calcium in large luteal cells. Similarly, PGE2 also induced increases in free intracellular calcium but required doses 20-fold greater than PGF2α. When PGE2 (1, 10 or 100 nM) was incubated with PGF2α (100 nM) increases in free intracellular calcium induced by PGF2α were attenuated (P<0.05) when measured 5 min, but not at 30 min, after initiation of treatment. The observed decrease in the concentration of free intracellular calcium at 5 min in response to PGF2α was the result of fewer cells responding to PGF2α. In addition, the concentrations of free intracellular calcium attained in the cells that did respond was reduced 25% compared to cells treated with PGF2α alone. Thus, part of the luteal protective actions of PGE2 appears to involve an inhibition of the early (5 min) increase in free intracellular calcium induced by PGF2α. 相似文献
11.
Douglas J. Bolt 《Prostaglandins & other lipid mediators》1979,18(3):387-396
The ability of human chorionic gonadotropin (HCG) to reduce the luteolytic effect of prostaglandin (PGF2α) was demonstrated in cycling ewes. As expected, treatment with 10 mg of PGF2α alone on Day 10 of the estrous cycle exerted a potent negative effect on the function and structure of corpus luteum (CL) as indicated by reduced plasma progesterone, CL progesterone, and CL weight. However, the identical PGF2α treatment failed to significantly reduce either luteal function or luteal weight when administered to ewes that were also treated with HCG on Days 9 and 10 of the estrous cycle. Treatment with HCG alone had a positive effect on CL as indicated by increased plasma progesterone, CL progesterone, and CL weight. Treatment with HCG did not render the CL totally insensitive to the negative effects of PGF2α because plasma progesterone was reduced when the dose of PGF2α was doubled. Whether CL regressed or continued to function after treatment with both HCG and PGF2α appeared to depend upon a balance between the positive and negative effects of the two hormones. 相似文献
12.
W.F. Williams G.S. Lewis W.W. Thatcher C.S. Underwood 《Prostaglandins & other lipid mediators》1983,25(6):891-899
On day 17 postestrus or postmating, heifers were given intrauterine injections of saline (2 pregnant, 2 non-pregnant) or 200 μg PGF2α (7 pregnant, 6 nonpregnant) through cannulae installed surgically into the uterine horn ipsilateral to the corpus luteum bearing ovary. Jugular blood samples were collected prior to the laparotomy at which the cannulae were installed during surgery, and for 90 min following the intrauterine injection. Plasma was assayed for progesterone and 13,14-dihyro-15-keto-PGF2α )PGFM). Laparotomies were reopened to confirm proper cannula placement and to determine if blastocysts were present in mated heifers. Concentrations of PGFM were higher in pregnant compared to nonpregnant heifers during the presurgery (68
26
24
26 pg/ml; P < 0.25) and surgery (186
47
65
17 pg/ml; P < .05) periods. Pregnancy status did not alter the mean concentrations of PGFM (pregnant, 554
70 pg/ml; nonpregnant, 422
81 pg/ml) or the half-life of its decline in concentration (18 min) following intrauterine injection of PGF2α. Pregnancy at 17 days in cattle does not appear to influence PGF2α transport from the uterine lumen or its metabolism in the uterus or elsewhere in response to an acute intrauterine injection. 相似文献
13.
John F. Gerkens John G. Gerber David G. Shand Robert A. Branch 《Prostaglandins & other lipid mediators》1978,16(5):815-823
Prostaglandins (PG)I2, PGE2 and 6-keto PGF1α were infused directly into the gastric arterial supply at 10−9, 10−8 and 10−7 g/kg/min during an intra-gastric artery pentagastrin infusion in anesthetized dogs. 6-keto PGF1α was also infused at 10−6 g/kg/min. Gastric arterial blood flow was measured continuously with a non-cannulating electromagnetic flow probe and gastric acid collected directly from the stomach. PGI2 and PGE2 produced similar dose-dependent increases in blood flow with an increase of more than four-fold at the highest dose. Both PGs inhibited acid output over this dose range with PGE2 having 10 times the potency of PGI2. 6-keto PGF1α was at least 1000 times less active than PGI2 or PGE2 at increasing blood flow and failed to inhibit acid output even at 10−6 g/kg/min. 相似文献
14.
Preliminary characterization indicated the presence of separate prostaglandin (PG)E1 and (PG)F2α binding sites in membrane fractions prepared from bovine corpora lutea. These differ in the rate and temperature dependence of the specific binding. Equilibrium binding data indicate the apparent dissociation constants as 1.32 × 10−9M and 2.1 × 10−8M for PGE1 and PGF2α, respectively. Competition of several natural prostaglandins for the PGE1 and PGF2α bovine luteal specific binding sites indicates specificity for the 9-keto or 9α-hydroxyl moiety, respectively. Differences in relative ability to inhibit 3H-PG binding were found due to sensitivity to the absence or presence of the 5,6-cis-double bond as well.Bovine luteal function was affected following treatment of heifers with 25 mg PGF2α as measured by reduced estrous cycle length, decreased corpus luteum size and significantly decreased plasma progesterone levels. In contrast, treatment with 25 mg PGE1 resulted in cycle lengths comparable to those of non-treated herdmates with no apparent modification in corpus luteum size. However, plasma progesterone levels were increased significantly following PGE1 treatment compared to pretreatment values. In so far as data obtained
on PGF2α relative binding affinity to the bovine CL can be compared to data obtained independently
on PGF2α induced luteolysis in the bovine, PGF2α relative binding to the CL and luteolysis appeared to be associated. By similar reasoning, there was no apparent relationship between PGE1 relative binding affinity in the luteal fractions and luteolysis in estrous cyclic cattle. 相似文献
15.
H.D. Hafs T.M. Louis J.N. Stellflug E.M. Convey J.H. Britt 《Prostaglandins & other lipid mediators》1975,10(6)
Two experiments were conducted to determine whether the increased serum LH which occurs within 12 hr after a luteolytic dose of PGF2α is dependent upon changes in progesterone or estradiol secretion. In the first experiment, exogenous progesterone abolished the increase in serum LH caused by a subcutaneous injection of 25 mg PGF2α in diestrous heifers, but not in ovariectomized heifers. In the second experiment, progesterone pessaries were removed at 6 hr after a subcutaneous injection of 25 mg PGF2α. LH remained at pre-PGF2α values while the pessaries were in place, but began to increase within 1 hr after they were removed. Blood estradiol also remained at pre-PGF2α values until the pessaries were removed, and began to increase at 2 hr after pessary removal. We conclude that the increase in serum LH within 12 hr after PGF2α treatment in diestrous cattle is dependent upon withdrawal of progesterone; it is not due to increased serum estradiol. 相似文献
16.
The role of progesterone in regulation of uteroovarian venous concentrations of prostaglandins F2 α (PGF2α) and E2 (PGE2) during days 13 to 16 of the ovine estrous cycle or early pregancy was examined. At estrus, ewes were either mated to a fertile ram or unmated. On day 12 postesturus, ewes were laparotomized and a catheter was inserted into a uteroovarian vein. Six mated and 7 unmated ewes received no further treatment. Fifteen mated and 13 unmated ewes were ovariectomized on day 12 and of these, 7 mated and 5 unmated ewes were given 10 mg progesteron sc and an intravaginal pessary containing 30 mg of progesterone. Uteroovarian venous samples were collected every 15 min for 3 h on days 13 to 16 postestrus. Mating resulted in higher mean daily concentrations of PGE2 in the uterovarian vein than in unmated ewes. Ovariectomy prevented the rise in PGE2 with day in mated ewes but had no effect in unmated ewes. Progesterone treatment restored PGE2 in ovariectomized, mated ewes with intact embros. Mating had no effect on mean daily concentrations of PGF2α or the patterns of the natural logarithm (ln) of the invariance of PGF2α. Ovariectomy resulted in higher mean concentrations and ln invariances of PGF2α on day 13 and lower mean concentrations and ln invariances of PGF2α on days 15 and 16. Replacement with progesterone prevented these changes in patters of mean concentrations and ln variances of PGF2α following ovariectomy. It is concluded that progesterone regulates the release of PGF2α from the uterus, maintaining high concentrations while also preventing the occurrence of the final peaks of PGF2α which are seen with falling concentrations of progesterone. This occurs in both pregnant and non-pregnant ewes. Progesterone is also needed to maintain increasing concentrations of PGE2 in mated ewes. 相似文献
17.
Preliminary characterization indicated the presence of separate prostaglandin (PG)E1 and (PG)F2α binding sites in membrane fractions prepared from bovine corpora lutea. These differ in the rate and temperature dependence of the specific binding. Equilibrium binding data indicate the apparent dissociation constants as 1.32 × 10−9M and 2.1 × 10−8M for PGE1 and PGF2α, respectively. Competition of several natural prostaglandins for the PGE1 and PGF2α bovine luteal specific binding sites indicates specificity for the 9-keto or 9α-hydroxyl moiety, respectively. Differences in relative ability to inhibit 3H-PG binding were found due to sensitivity to the absence or presence of the 5,6-cis-double bond as well.Bovine luteal function was affected following treatment of heifers with 25 mg PGF2α as measured by reduced estrous cycle length, decreased corpus luteum size and significantly decreased plasma progesterone levels. In contrast, treatment with 25 mg PGE1 resulted in cycle lengths comparable to those of non-treated herdmates with no apparent modification in corpus luteum size. However, plasma progesterone levels were increased significantly following PGE1 treatment compared to pretreatment values. In so far as data obtained in vitro on PGF2α relative binding affinity to the bovine CL can be compared to data obtained independently in vitro on PGF2α induced luteolysis in the bovine, PGF2α relative binding to the CL and luteolysis appeared to be associated. By similar reasoning, there was no apparent relationship between PGE1 relative binding affinity in the luteal fractions and luteolysis in estrous cyclic cattle. 相似文献
18.
Pregnant hamsters were administered (SC) prostaglandin or vehicle on the morning of the 4th day of pregnancy. Serum progesterone was significantly depressed (p<.01) at 0.5, 2, and 6 hours after treatment with 100 μg PGF2α. Serum progesterone levels were unchanged 2 hours and 6 hours after treatment with 100 μg PGF2β and 2 hours after treatment with 1 mg PGF2β. Progesterone levels were depressed to less than 1 ng/ml 6 hours after treatment with 1 mg PGF2β. The specific uptake of 3H-PGF2α in whole hamster corpora lutea was significantly depressed 2 hours and 6 hours following 100 μg PGF2α treatment. A 15% depression in specific uptake occurred 0.5 hour post-treatment. Treatment with 100 μg PGF2β resulted in no change. Administration of 1 mg PGF2β resulted in depressed 3H-PGF2α uptake at both 2 and 6 hours post-treatment.Prostacyclin (PGI2) treatment resulted in no change in either 3H-PGF2α specific uptake or serum progesterone 2 hours after 100 μg treatment SC. These parameters were both reduced approximately 30% 6 hours post-treatment. Treatment with 6-keto-PGF1α resulted in a complete lack of measurable 3H-PGF2α uptake and serum progesterone levels less than 1 ng/ml at both 2 and 6 hours after treatment with 1 mg SC. 相似文献
19.
The effects of PGF2α infusion in a dose of 25 μg/min for 5 hours on serum levels of estradiol-17β, progesterone, LH, FSH, TSH and prolactin, and on the pituitary hormone responsiveness to LRH and TRH were studied in 10 apparently healthy cycling women in the mid-luteal phase. No systematic alteration was seen in the pituitary and ovarian hormone levels during PGF2α infusion, and the pituitary hormone responses to releasing hormones were unaffected. Ovarian steroid production increased in response to increased gonadotropin levels after LRH injection during PGF2α administration. These results confirm that PGF2α is not luteolytic in humans and no apparent relationship between PGF2α and pituitary hormone secretion exists. 相似文献
20.
Y.S. Weems D.L. Vincent K.D. Nusser Y. Tanaka K. Miller-Patrick K.S. Ledgerwood C.W. Weems 《Prostaglandins & other lipid mediators》1993,46(3)
Vehicle or 8 or 16 mg of PGF2α per 58 kg body weight was given intramuscularly to intact, hysterectomized or ovariectomized 90–100 day pregnant ewes in three separate experiments. Both doses of PGF2α increased PGF2α in ovarian venous plasma compared with controls at 72 hr post treatment in intact (P≤0.05) but did not in hysterectomized (P≥0.05) 90–100 day pregnant ewes. Concentrations of PGE in ovarian venous blood of intact ewes did not differ (P≥0.05) between treatment groups and were equivalent to concentrations of PGE determined in uterine venous plasma. PGE was decreased in ovarian venous plasma by PGF2α in hysterectomized ewes (P≤0.07). PGE in uterine venous plasma averaged 6 ng/ml over the 72-hr treatment period in intact and ovariectomized 90–100 day pregnant ewes and was 12 fold greater (P≤0.05) than PGF2α which averaged 500 pg/ml in uterine venous plasma. Both PGF2α and PGE increased (P≤0.05) by 64 hr in uterine venous plasma of the 8 mg PGF2α — treated intact pregnant ewes. A significant quadratic increase (P≤0.05) was observed for PGF2α and PGE in the vehicle and both PGF2α treatment groups of intact ewes at the end of the 72-hr sampling period. It is concluded that the uterus and ovaries secrete significant quantities of PGE but little PGF2α during midgestation. In addition, PGF2α increased uterine secretion of PGE
. PGE may be a placental stimulator of ovine placental secretion of progesterone or PGE may protect placental steroidogenesis from actions of PGF2α. 相似文献